In the normal human heart, the sinus node, generally located near the junction of the superior vena cava and the right atrium, constitutes the primary natural pacemaker initiating rhythmic electrical excitation of the heart chambers. The cardiac impulse arising from the sinus node is transmitted to the two atrial chambers, causing a depolarization known as a P-wave and the resulting atrial chamber contractions. The excitation pulse is further transmitted to and through the ventricles via the atrioventricular (A-V) node and a ventricular conduction system causing a depolarization known as an R-wave and the resulting ventricular chamber contractions.
Disruption of this natural pacemaking and conduction system as a result of aging or disease can be successfully treated by artificial cardiac pacing using implantable cardiac stimulation devices, including pacemakers and implantable defibrillators, which deliver rhythmic electrical pulses or anti-arrhythmia therapies to the heart at a desired energy and rate. A cardiac stimulation device is electrically coupled to the heart by one or more leads possessing one or more electrodes in contact with the heart muscle tissue (myocardium).
Stimulation may be delivered to the atrial and/or the ventricular heart chambers depending on the location and severity of the conduction disorder. In dual chamber, demand-type pacemakers, commonly referred to as DDD pacemakers, an atrial channel and a ventricular channel each include a sense amplifier to detect cardiac activity in the respective chamber and an output circuit for delivering stimulation pulses to the respective chamber. If the atrial channel does not detect an intrinsic atrial depolarization signal (a P-wave), a stimulating pulse will be delivered to depolarize the atrium and cause contraction. Following either a detected P-wave or an atrial pacing pulse, the ventricular channel attempts to detect a depolarization signal in the ventricle, known as an R-wave. If no R-wave is detected within a defined atrial-ventricular interval (AV interval or delay), a stimulation pulse is delivered to the ventricle to cause ventricular contraction. In this way, atrial-ventricular synchrony is maintained by coordinating the delivery of ventricular output in response to a sensed or paced atrial event.
A stimulation pulse delivered to the myocardium must be of sufficient energy to depolarize the tissue, thereby causing a contraction, a condition commonly known as “capture.” In early pacemakers, a fixed, high-energy pacing pulse was delivered to ensure capture. While this approach is straightforward, it quickly depletes battery energy and can result in patient discomfort due to extraneous stimulation of surrounding skeletal muscle tissue.
The capture “threshold” is defined as the lowest stimulation pulse energy at which consistent capture occurs. By stimulating the heart chambers at or just above threshold, comfortable and effective cardiac stimulation is provided without unnecessary depletion of battery energy. Threshold, however, is extremely variable from patient-to-patient due to variations in electrode systems used and the electrode positioning. In addition, there are physiological and anatomical variations of the heart itself, and so on. Furthermore, threshold will vary over time within a patient as, for example, fibrotic encapsulation of the electrode occurs during the first few weeks after surgery. Fluctuations may even occur over the course of a day or with changes in medical therapy or disease state.
Hence, techniques for monitoring the cardiac activity following delivery of a stimulation pulse have been incorporated in modern pacemakers in order to verify that capture has indeed occurred. Typically, the internal myocardial electrogram (EGM) signals received on cardiac sensing electrodes are sampled and processed in a way that allows detection of an “evoked response” following delivery of a stimulation pulse. If a loss of capture is detected, that is no evoked response is detected, by such “capture-verification” algorithms, a high-energy safety pulse that will ensure capture can be immediately delivered to prevent a missed heart beat. After which, the cardiac pacing device automatically performs a threshold test in order to re-determine the capture threshold and automatically adjust the stimulation pulse energy to be just above threshold. This approach, called “automatic capture”, improves the cardiac stimulation device performance in at least two ways: 1) by verifying that the stimulation pulse delivered to the patient's heart has been effective; and 2) greatly increasing the device's battery longevity by conserving the energy used to generate stimulation pulses.
In dual chamber stimulation devices, therefore, accurate sensing of both evoked responses and the intrinsic deflection of the naturally occurring cardiac events, also referred to as “intrinsic” events, is crucial for achieving atrial-ventricular synchrony. However, sometimes stimulation pulses generated by, for example, the atrial channel of the pacemaker may be detected by the sensing circuitry of the ventricular channel and mistakenly identified as a naturally occurring ventricular event. This phenomenon is commonly referred to as “crosstalk.” An atrial stimulation pulse mistakenly detected by the ventricular channel will cause ventricular stimulation output to be inhibited when in fact stimulation is needed, resulting in a “missed beat” or asystole, an undesirable situation.
A common approach for preventing crosstalk is to apply a “blanking interval” to the sensing circuitry of the channel in which crosstalk is anticipated. For example, during application of an atrial stimulation pulse, and for a short time thereafter, the ventricular sensing circuitry is disengaged to prevent the detection of the atrial stimulation pulse and the associated afterpotential signal.
The blanking interval is preferably kept as short as possible to prevent undersensing of natural cardiac events, but it must be long enough to prevent crosstalk. Undersensing of a naturally occurring cardiac event may cause the pacemaker to apply an inappropriate stimulus to the heart. For example, if the pacemaker fails to detect a late-cycle ventricular depolarization because the intrinsic deflection of the EGM occurred during the ventricular blanking interval, an unnecessary stimulation pulse will be delivered to the ventricle. This stimulation pulse may fail to capture the heart because it is delivered during the physiologic refractory period following the native depolarization.
The loss of capture will invoke the automatic capture feature causing a high-energy, back-up pulse to be delivered. This back-up pulse could be delivered coincidentally with the repolarization phase of the myocardium, represented by the T-wave portion of the ECG signal. Delivery of a high-energy stimulation pulse that is certain to capture the heart during the T-wave can induce a potentially life-threatening ventricular tachycardia in a patient susceptible to cardiac arrhythmias. Thus, the automatic capture feature, which is intended as a safety feature, may have an adverse effect even during normal operation of the stimulation device. It is therefore extremely important to minimize ventricular stimulation competition with intrinsic ventricular activity due to blanking period ventricular undersensing as just described.
One approach to avoiding T-wave stimulation that might occur as a result of ventricular fusion or pseudofusion which can be interpreted by the automatic capture algorithm as noncapture resulting in delivery of the high-output back-up pulse is to extend the AV interval on the next cycle. If the presumed loss of capture was actually due to fusion with intact AV nodal conduction, the native ventricular complex will be sensed and inhibit the subsequent ventricular output. However, this approach does not remedy the problem of blanking period ventricular undersensing of ventricular depolarizations.
A method for minimizing the blanking period to avoid blanking period undersensing while still preventing crosstalk involves a total blanking period that includes an absolute blanking period and a relative blanking period. The absolute blanking interval may be kept very short to prevent sensing of afterpotential signals associated with the atrial stimulation pulse. The absolute blanking period is followed by a relative blanking period, during which any sensed events are presumed to be residual effects of crosstalk. If no event is detected during the relative refractory period, the blanking period is terminated. An event detection during the relative blanking period will therefore restart a second blanking period until the crosstalk signal has ended. This approach is effective in minimizing the ventricular blanking period in the absence of crosstalk while still preventing crosstalk from occurring when a residual signal can be detected on the ventricular channel.
The situation of a true intrinsic deflection associated with a native cardiac depolarization occurring during the absolute blanking period, and going undetected, has not been fully addressed heretofore. What is needed is a method to determine if a loss of capture event is actually the result of blanking period ventricular undersensing. Blanking period ventricular undersensing may have caused delivery of a ventricular output at a time when capture is not possible, resulting in a loss of capture and the subsequent delivery of a back-up pulse that may be effective since it is delivered later in the cycle. If blanking period ventricular undersensing is suspected, a method for adjusting the stimulation device operating parameters to minimize the occurrences of blanking period ventricular undersensing is desirable. In this way, the potential for triggering a life-threatening tachycardia by unnecessarily stimulating on a T-wave is reduced.